Zhao Xin, Chen Xinru, Xin Xiangyang
Department of Ophthalmology, Baogang Hospital of Inner Mongolia, Baotou, 014010, Inner Mongolia, China.
Department of Ophthalmology, Baotou Central Hospital, Baotou, 014040, Inner Mongolia, China.
Int Ophthalmol. 2025 May 9;45(1):183. doi: 10.1007/s10792-025-03540-3.
The mechanism of age-related macular degeneration (AMD) is a complex illness that is not fully understood. Therefore, the aim of this study was to investigate the expression patterns of miR-6837-3p in retinal epithelial cells.
HO was used to treat ARPE-19 cells for 2, 4 and 6 h to mimic the in vivo environment of AMD. MiR inhibitors and mimics were used to inhibit or overexpress miR-6837-3p in HO-treated ARPE-19 cells, respectively. Then, CCK8 assay, flow cytometry, and wound healing assays were conducted to assess the effects of miR-6837-3p on the behaviors of ARPE-19 cells, including cell growth, apoptosis, cycle progression, and migration. Finally, microRNA database prediction and luciferase reporter assays were used to demonstrate that miR-6837-3p targets the downstream gene E2F6.
HO induced a decrease in cell viability and an increase in ROS levels in a time-dependent manner. Additionally, overexpression of miR-6837-3p increased cell viability and suppressed apoptosis in ARPE-19 cells treated with HO. Meanwhile, increased miR-6837-3p promoted cell cycle progression and cell migration of ARPE-19 cells. Finally, miR-6837-3p exerted anti-apoptosis and anti-oxidative stress effects by inhibiting the expression of E2F6 in ARPE-19 cells.
The MiR-6837-3p/E2F6 axis might be a target for the treatment of AMD to improve ARPE-19 cell function.
年龄相关性黄斑变性（AMD）是一种机制复杂且尚未完全明确的疾病。因此，本研究旨在探究视网膜上皮细胞中miR-6837-3p的表达模式。
采用过氧化氢（HO）处理ARPE-19细胞2、4和6小时，以模拟AMD的体内环境。分别使用miR抑制剂和模拟物抑制或过表达HO处理的ARPE-19细胞中的miR-6837-3p。然后，进行CCK8检测、流式细胞术和伤口愈合检测，以评估miR-6837-3p对ARPE-19细胞行为的影响，包括细胞生长、凋亡、周期进程和迁移。最后，利用微小RNA数据库预测和荧光素酶报告基因检测来证明miR-6837-3p靶向下游基因E2F6。
HO以时间依赖性方式诱导细胞活力下降和活性氧水平升高。此外，miR-6837-3p过表达可提高HO处理的ARPE-19细胞的活力并抑制其凋亡。同时，miR-6837-3p的增加促进了ARPE-19细胞的细胞周期进程和细胞迁移。最后，miR-6837-3p通过抑制ARPE-19细胞中E2F6的表达发挥抗凋亡和抗氧化应激作用。
MiR-6837-3p/E2F6轴可能是治疗AMD以改善ARPE-19细胞功能的靶点。
